Signal transduction in primary human T lymphocytes in altered gravity – results of the MASER-12 suborbital space flight mission

Cell Communication and Signaling

Research

Claudia Crescio¹  Antonella Pantaleo¹  Proto Pippia¹  Angela Saba¹  Christian Secchi²  Cora Sandra Thiel³  Swantje Hauschild³  Katrin Paulsen³  Isabell Buttron³  Svantje Tauber⁴  Oliver Ullrich⁵  Augusto Cogoli⁶ 

[1] Department of Biomedical Sciences, University of Sassari, Via Muroni, 25, 07100, Sassari, Italy;Department of Medicine, University of Verona, Piazzale A. Stefani 1, 37126, Verona, Italy;Institute of Anatomy, Faculty of Medicine, University of Zurich, Winterthurerstrasse 190, CH-8057, Zurich, Switzerland;Institute of Anatomy, Faculty of Medicine, University of Zurich, Winterthurerstrasse 190, CH-8057, Zurich, Switzerland;Department of Machine Design, Engineering Design and Product Development, Institute of Mechanical Engineering, Otto-von-Guericke-University Magdeburg, Universitätsplatz 2, D-39106, Magdeburg, Germany;Institute of Anatomy, Faculty of Medicine, University of Zurich, Winterthurerstrasse 190, CH-8057, Zurich, Switzerland;Department of Machine Design, Engineering Design and Product Development, Institute of Mechanical Engineering, Otto-von-Guericke-University Magdeburg, Universitätsplatz 2, D-39106, Magdeburg, Germany;Zurich Center for Integrative Human Physiology (ZIHP), University of Zurich, Zurich, Switzerland;Zero-G Life Tec, Riedhofstrasse 273, 8049, Zurich, Switzerland;

关键词: T cell activation;    Microgravity;    Gravi-sensitivity;    Hypergravity;    Space flight;   

DOI  :  10.1186/1478-811X-11-32

 received in 2013-01-10, accepted in 2013-04-18,  发布年份 2013

来源: Springer

【 摘 要 】

We investigated the influence of altered gravity on key proteins of T cell activation during the MASER-12 ballistic suborbital rocket mission of the European Space Agency (ESA) and the Swedish Space Cooperation (SSC) at ESRANGE Space Center (Kiruna, Sweden). We quantified components of the T cell receptor, the membrane proximal signaling, MAPK-signaling, IL-2R, histone modifications and the cytoskeleton in non-activated and in ConA/CD28-activated primary human T lymphocytes. The hypergravity phase during the launch resulted in a downregulation of the IL-2 and CD3 receptor and reduction of tyrosine phosphorylation, p44/42-MAPK phosphorylation and histone H3 acetylation, whereas LAT phosphorylation was increased. Compared to the baseline situation at the point of entry into the microgravity phase, CD3 and IL-2 receptor expression at the surface of non-activated T cells were reduced after 6 min microgravity. Importantly, p44/42-MAPK-phosphorylation was also reduced after 6 min microgravity compared to the 1g ground controls, but also in direct comparison between the in-flight μg and the 1g group. In activated T cells, the reduced CD3 and IL-2 receptor expression at the baseline situation recovered significantly during in-flight 1g conditions, but not during microgravity conditions. Beta-tubulin increased significantly after onset of microgravity until the end of the microgravity phase, but not in the in-flight 1g condition. This study suggests that key proteins of T cell signal modules are not severely disturbed in microgravity. Instead, it can be supposed that the strong T cell inhibiting signal occurs downstream from membrane proximal signaling, such as at the transcriptional level as described recently. However, the MASER-12 experiment could identify signal molecules, which are sensitive to altered gravity, and indicates that gravity is obviously not only a requirement for transcriptional processes as described before, but also for specific phosphorylation / dephosphorylation of signal molecules and surface receptor dynamics.

【 授权许可】

Unknown   
© Tauber et al.; licensee BioMed Central Ltd. 2013. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.